Role of EGR1 in hippocampal synaptic enhancement induced by tetanic stimulation and amputation

Feng Wei, Zao C. Xu, Zhican Qu, Jeffrey Milbrandt, Min Zhuo

Research output: Contribution to journalArticle

91 Citations (Scopus)

Abstract

Hippocampal neurons fire spikes when an animal is at a particular location or performs certain behaviors in a particular place, providing a cellular basis for hippocampal involvement in spatial learning and memory. In a natural environment, spatial memory is often associated with potentially dangerous sensory experiences such as noxious or painful stimuli. The central sites for such pain-associated memory or plasticity have not been identified. Here we present evidence that excitatory glutamatergic synapses within the CA1 region of the hippocampus may play a role in storing pain-related information. Peripheral noxious stimulation induced excitatory postsynaptic potentials (EPSPs) in CA1 pyramidal cells in anesthetized animals. Tissue/nerve injury caused a rapid increase in the level of the immediate- early gene product Egr1 (also called NGFI-A, Krox24, or zif/268) in hippocampal CA1 neurons. In parallel, synaptic potentiation induced by a single tetanic stimulation (100 Hz for 1 s) was enhanced after the injury. This enhancement of synaptic potentiation was absent in mice lacking Egr1. Our data suggest that Egr1 may act as an important regulator of pain-related synaptic plasticity within the hippocampus.

Original languageEnglish
Pages (from-to)1325-1333
Number of pages9
JournalJournal of Cell Biology
Volume149
Issue number7
DOIs
StatePublished - Jun 26 2000

Fingerprint

Amputation
Pain
Hippocampus
Neurons
Nerve Tissue
Neuronal Plasticity
Immediate-Early Genes
Pyramidal Cells
Excitatory Postsynaptic Potentials
Wounds and Injuries
Synapses
Spatial Memory

Keywords

  • Egr1
  • Hippocampus
  • LTP
  • NMDA
  • Pain

ASJC Scopus subject areas

  • Cell Biology

Cite this

Role of EGR1 in hippocampal synaptic enhancement induced by tetanic stimulation and amputation. / Wei, Feng; Xu, Zao C.; Qu, Zhican; Milbrandt, Jeffrey; Zhuo, Min.

In: Journal of Cell Biology, Vol. 149, No. 7, 26.06.2000, p. 1325-1333.

Research output: Contribution to journalArticle

Wei, Feng ; Xu, Zao C. ; Qu, Zhican ; Milbrandt, Jeffrey ; Zhuo, Min. / Role of EGR1 in hippocampal synaptic enhancement induced by tetanic stimulation and amputation. In: Journal of Cell Biology. 2000 ; Vol. 149, No. 7. pp. 1325-1333.
@article{d3163adf6fcf4da389cbc2f28740d9e5,
title = "Role of EGR1 in hippocampal synaptic enhancement induced by tetanic stimulation and amputation",
abstract = "Hippocampal neurons fire spikes when an animal is at a particular location or performs certain behaviors in a particular place, providing a cellular basis for hippocampal involvement in spatial learning and memory. In a natural environment, spatial memory is often associated with potentially dangerous sensory experiences such as noxious or painful stimuli. The central sites for such pain-associated memory or plasticity have not been identified. Here we present evidence that excitatory glutamatergic synapses within the CA1 region of the hippocampus may play a role in storing pain-related information. Peripheral noxious stimulation induced excitatory postsynaptic potentials (EPSPs) in CA1 pyramidal cells in anesthetized animals. Tissue/nerve injury caused a rapid increase in the level of the immediate- early gene product Egr1 (also called NGFI-A, Krox24, or zif/268) in hippocampal CA1 neurons. In parallel, synaptic potentiation induced by a single tetanic stimulation (100 Hz for 1 s) was enhanced after the injury. This enhancement of synaptic potentiation was absent in mice lacking Egr1. Our data suggest that Egr1 may act as an important regulator of pain-related synaptic plasticity within the hippocampus.",
keywords = "Egr1, Hippocampus, LTP, NMDA, Pain",
author = "Feng Wei and Xu, {Zao C.} and Zhican Qu and Jeffrey Milbrandt and Min Zhuo",
year = "2000",
month = "6",
day = "26",
doi = "10.1083/jcb.149.7.1325",
language = "English",
volume = "149",
pages = "1325--1333",
journal = "Journal of Cell Biology",
issn = "0021-9525",
publisher = "Rockefeller University Press",
number = "7",

}

TY - JOUR

T1 - Role of EGR1 in hippocampal synaptic enhancement induced by tetanic stimulation and amputation

AU - Wei, Feng

AU - Xu, Zao C.

AU - Qu, Zhican

AU - Milbrandt, Jeffrey

AU - Zhuo, Min

PY - 2000/6/26

Y1 - 2000/6/26

N2 - Hippocampal neurons fire spikes when an animal is at a particular location or performs certain behaviors in a particular place, providing a cellular basis for hippocampal involvement in spatial learning and memory. In a natural environment, spatial memory is often associated with potentially dangerous sensory experiences such as noxious or painful stimuli. The central sites for such pain-associated memory or plasticity have not been identified. Here we present evidence that excitatory glutamatergic synapses within the CA1 region of the hippocampus may play a role in storing pain-related information. Peripheral noxious stimulation induced excitatory postsynaptic potentials (EPSPs) in CA1 pyramidal cells in anesthetized animals. Tissue/nerve injury caused a rapid increase in the level of the immediate- early gene product Egr1 (also called NGFI-A, Krox24, or zif/268) in hippocampal CA1 neurons. In parallel, synaptic potentiation induced by a single tetanic stimulation (100 Hz for 1 s) was enhanced after the injury. This enhancement of synaptic potentiation was absent in mice lacking Egr1. Our data suggest that Egr1 may act as an important regulator of pain-related synaptic plasticity within the hippocampus.

AB - Hippocampal neurons fire spikes when an animal is at a particular location or performs certain behaviors in a particular place, providing a cellular basis for hippocampal involvement in spatial learning and memory. In a natural environment, spatial memory is often associated with potentially dangerous sensory experiences such as noxious or painful stimuli. The central sites for such pain-associated memory or plasticity have not been identified. Here we present evidence that excitatory glutamatergic synapses within the CA1 region of the hippocampus may play a role in storing pain-related information. Peripheral noxious stimulation induced excitatory postsynaptic potentials (EPSPs) in CA1 pyramidal cells in anesthetized animals. Tissue/nerve injury caused a rapid increase in the level of the immediate- early gene product Egr1 (also called NGFI-A, Krox24, or zif/268) in hippocampal CA1 neurons. In parallel, synaptic potentiation induced by a single tetanic stimulation (100 Hz for 1 s) was enhanced after the injury. This enhancement of synaptic potentiation was absent in mice lacking Egr1. Our data suggest that Egr1 may act as an important regulator of pain-related synaptic plasticity within the hippocampus.

KW - Egr1

KW - Hippocampus

KW - LTP

KW - NMDA

KW - Pain

UR - http://www.scopus.com/inward/record.url?scp=0034717750&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0034717750&partnerID=8YFLogxK

U2 - 10.1083/jcb.149.7.1325

DO - 10.1083/jcb.149.7.1325

M3 - Article

VL - 149

SP - 1325

EP - 1333

JO - Journal of Cell Biology

JF - Journal of Cell Biology

SN - 0021-9525

IS - 7

ER -